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OXIDATIVE STRESS PREDICTS HIP FRACTURE Elizabeth Hofheinz, M.P.H., M.Ed. • Thu, August 28th, 2014 http://ryortho.c...om/breaking/oxidative-stress-predicts-hip-fracture/ Researchers from the University of Cincinnati (UC), Harvard School of Public Health, and Harvard Medical School have found that oxidative stress is a significant predictor for hip fracture in postmenopausal women. The study appears online ahead of print in the Journal of Bone and Mineral Research. The research was led by Tianying Wu, M.D., Ph.D., an assistant professor in the UC College of Medicine Department of Environmental Health, and Shuman Yang, a postdoctoral fellow in the department. The team evaluated participants from the Nurses’ Health Study, and measured oxidative stress by noting fluorescent oxidation products (FlOP) in blood plasma. “To our knowledge, this is the first prospective study among postmenopausal women demonstrating that oxidative stress was a significant predictor for hip fracture,” said Dr. Wu in the August 14, 2014 news release. According to the news release, a total of 996 women aged 60 or older were measured at baseline blood collection (1989-1990). “Plasma FlOPs were measured at three excitation/emission wavelengths: 360/420 nm (nanometers), named as FlOP_360; 320/420 nm, named as FlOP_320; and 400-475 nm, named as FlOP_400. FlOP_360 represents oxidation products that are generated from oxidized phospholipids or from lipid oxidation products reacting with proteins. FlOP_320 is formed when oxidation products such as lipid hydroperoxides, aldehydes and ketones react with DNA in the presence of metals. FlOP_400 reflects the interaction between malondialdehyde (a specific marker for lipid oxidation), proteins and phospholipids.” “Of the three wavelengths, researchers found that baseline levels of FlOP_320 products predicted risk of future hip fracture in the study cohort. (No association was found with FlOP_360 and FlOP_400.) Increased FlOP_320 was associated with greater risk of hip fracture; women in the upper 30% of FlOP_320 readings were found to have 2.67 times the risk of hip fractures of those in the bottom 30%.” “Because FlOP_320 is generated in the presence of metals, its strong association with hip fractures may reflect the co-existing effect of reactive oxygen species and heavy metals,” says Dr. Wu, who notes that the other FlOP products can be generated without metals. Dr. Wu told OTW, “If our results are confirmed in larger studies, FlOP_320 may potentially used as a marker for screening individuals are at risk for hip fracture in addition to DEXA scan.”

Amyotrophic lateral sclerosis (ALS) is characterized by the progressive loss of motoneurons and degradation of the neuromuscular junctions (NMJ). Consistent with the dying-back hypothesis of motoneuron degeneration the decline in synaptic function initiates from the presynaptic terminals in ALS. Oxidative stress is a major contributory factor to ALS pathology and affects the presynaptic transmitter releasing machinery. Indeed, in ALS mouse models nerve terminals are sensitive to reactive oxygen species (ROS) suggesting that oxidative stress, along with compromised mitochondria and increased intracellular Ca(2+) amplifies the presynaptic decline in NMJ. This initial dysfunction is followed by a neurodegeneration induced by inflammatory agents and loss of trophic support. To develop effective therapeutic approaches against ALS, it is important to identify the mechanisms underlying the initial pathological events. Given the role of oxidative stress in ALS, targeted antioxidant treatments could be a promising therapeutic approach. However, the complex nature of ALS and failure of monotherapies suggest that an antioxidant therapy should be accompanied by anti-inflammatory interventions to enhance the restoration of the redox balance. KEYWORDS: ALS; ROS; neurodegeneration; neuromuscular junction; oxidative stresshttp://www.ncbi.nlm.nih.gov/pubmed/24860432

August 18, 2014

In an Ecosystem Within Us, Microbes Evolved to Sway Food Choices

It sounds like science fiction, but it seems that bacteria within us – which outnumber our own cells about 100-fold – may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.

In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.

A Power Struggle Inside the Gut

Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem – our digestive tracts – they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.

Are we at the mercy of our gut bacteria? The above image illustrates how microbes can "pull our strings," driving us to crave foods that give them the nutrients they need, including fat and sugar.

While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.

“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”

Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.

“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”

There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.

The Connection Between Digestive Tract and Brain

Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.

Athena Aktipis, PhD

Carlo Maley, PhD

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.

In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.

Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?

The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.

Implications for Obesity, Diabetes and even Cancer

The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago.

Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.

In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.

“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.

The co-authors’ BioEssays study was funded by the National Institutes of Health, the American Cancer Society, the Bonnie D. Addario Lung Cancer Foundation and the Institute for Advanced Study, in Berlin.

UC San Francisco (UCSF), now celebrating the 150th anniversary of its founding, is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.

August 07, 2014

Why is the western media not all over this? Where is CNN when you need them?

Ukraine's Security Service: Russian terrorists and militants planned a cynical terrorist attack against an Aeroflot civil aircraft (...Shot down Malaysian Flight MH17 instead)Valentyn Nalyvaychenko, Ukraine's Security Service Head: During the investigation of Malaysia Airlines Boeing-777 downing the law enforcement and intelligence bodies established that terrorists and militants have cynically planned the terrorist attack against Aeroflot civil aircraft, AFL-2074 Moscow-Larnaca, which was flying over the territory of Ukraine at that moment.

The Current Information Warfare (called Reflexive Control) used by Russia against Ukraine today

Distraction, by creating a real or imaginary threat to one of the enemy’s most vital locations (flanks, rear, etc.) during the preparatory stages of combat operations, thereby forcing him to reconsider the wisdom of his decisions to operate along this or that axis;

• Russian troops at the Ukrainian boarder

Strategic missile tests

Overload, by frequently sending the enemy a large amount of conflicting information;

• Russian spies in all levels of the Ukrainian government

• Russia Today TV and all Russian mass media outlets

Paralysis, by creating the perception of a specific threat to a vital interest or weak spot;

• Diversions in Lviv, Zakarpatia and on Maidan in Kyiv

Exhaustion, by compelling the enemy to carry out useless operations, thereby entering combat with reduced resources;

• Multiple small skirmishes and checkpoint controls in Luhansk and Donetsk

Deception, by forcing the enemy to reallocate forces to a threatened region during the preparatory stages of combat operations;

• Multiple small skirmishes and checkpoint controls in Luhansk and Donetsk

Division, by convincing the enemy that he must operate in opposition to coalition interests;

• Invasion of Crimea and passive army resistance

Pacification, by leading the enemy to believe that pre-planned operational training is occurring rather than offensive preparations, thus reducing his vigilance;

• Countless Russian training maneuvers at or near the Ukrainian boarder

Deterrence, by creating the perception of insurmountable superiority;

• Infographics on FB and the internet about the hardware superiority of the RF army vs the Ukrainian army

Provocation, by forcing him into taking action advantageous to your side;

• Many existing Ukrainian Parliamentary MP get bribes from Russia to allow contraband, narcotics and weapons to cross from Russia into Ukraine unimpeded

Overload, by dispatching an excessively large number of messages to the enemy during the preparatory period;

• Russian mass media

Suggestion, by offering information that affects the enemy legally, morally, ideologically, or in other areas;

• The Kremlin is trying to scare the EU with response sanctions: “This is just like war”

and

Pressure, by offering information that discredits the government in the eyes of its population.

• Russia Today and all Russian media outlets.

Local Oblast and village politicians and business owners get bribed by Russia to tow the Russian line.

We can play the Reflexive Control game in the West to topple Putin too. How?

I can think of at least a dozen tactics. Here is just one example that is starting to be put into play:

Imposing sanctions is the right strategy; what we haven’t got right is the objective of these sanctions-which should be to get the Russian Oligarchs who’ve been keeping Putin in power, or tolerating Putin in power, to throw the knockout punch against him.

Herbert E. Meyer, who served during the Reagan Administration as Special Assistant to the Director of Central Intelligence –William (Bill) Casey and Vice Chairman of the CIA's National Intelligence Council concludes: “That’s why the sanctions will work if Obama and his European counterparts will keep tightening the screws; if they keep making commerce more difficult for Russia’s serious business executives, for instance by blocking their access to capital, and if they keep making life more miserable for Russia’s playboy oligarchs, for instance by canceling their credit cards and denying landing rights to their private jets.” (cancelling boarding school privileges in the U.K. for about 4,000 Russian students from rich families or denying Oligarchs their yacht mooring privileges in London or the Riviera-disaster !!-WD}.

The West must send one clear message: Obama, Harper and European leaders must keep telling the Russians -- bluntly and publicly -- that all this will end the moment Vladimir Putin leaves the Kremlin for good.

August 04, 2014

Researchers at the University of California, San Diego School of Medicine report that dietary capsaicin – the active ingredient in chili peppers – produces chronic activation of a receptor on cells lining the intestines of mice, triggering a reaction that ultimately reduces the risk of colorectal tumors.

The findings are published in the August 1, 2014 issue of The Journal of Clinical Investigation.

The receptor or ion channel, called TRPV1, was originally discovered in sensory neurons, where it acts as a sentinel for heat, acidity and spicy chemicals in the environment. “These are all potentially harmful stimuli to cells,” said Eyal Raz, MD, professor of Medicine and senior author of the study. “Thus, TRPV1 was quickly described as a molecular ‘pain receptor.’ This can be considered to be its conventional function, which all takes place in the nervous system.”

But Raz and colleagues have found that TPRV1 is also expressed by epithelial cells of the intestines, where it is activated by epidermal growth factor receptor or EGFR. EGFR is an important driver of cell proliferation in the intestines, whose epithelial lining is replaced approximately every four to six days.

“A basic level of EGFR activity is required to maintain the normal cell turnover in the gut,” said Petrus de Jong, MD, first author of the study. “However, if EGFR signaling is left unrestrained, the risk of sporadic tumor development increases.”

The scientists discovered that TRPV1, once activated by the EGFR, initiates a direct negative feedback on the EGFR, dampening the latter to reduce the risk of unwanted growth and intestinal tumor development. They found that mice genetically modified to be TRPV1-deficient suffered higher-than-normal rates of intestinal tumor growths.

“These results showed us that epithelial TRPV1 normally works as a tumor suppressor in the intestines,” said de Jong. In addition, molecular studies of human colorectal cancer samples recently uncovered multiple mutations in the TRPV1 gene, though Raz noted that currently there is no direct evidence that TRPV1 deficiency is a risk factor for colorectal cancer in humans.

“A direct association between TRPV1 function and human colorectal cancer should be addressed in future clinical studies,” he said.

But if such proves to be the case, the current study suggests one potential remedy might be spicy capsaicin, which acts as an irritant in mammals, generating a burning sensation in contact with tissue. Capsaicin is already broadly used as an analgesic in topical ointments, where its properties as an irritant overwhelm nerves, rendering them unable to report pain for extended periods of time. It’s also the active ingredient in pepper spray.

The researchers fed capsaicin to mice genetically prone to developing multiple tumors in the gastrointestinal tract. The treatment resulted in a reduced tumor burden and extended the lifespans of the mice by more than 30 percent. The treatment was even more effective when combined with celecoxib, a COX-2 non-steroidal anti-inflammatory drug already approved for treating some forms of arthritis and pain.

“Our data suggest that individuals at high risk of developing recurrent intestinal tumors may benefit from chronic TRPV1 activation,” said Raz. “We have provided proof-of-principle.”

This research was supported, in part, by the Crohn’s and Colitis Foundation of America, the Prins Bernhard Cultural Foundation, the Scholten-Cordes Foundation, the Dr. Hendrick Muller Vaderlandsch Foundation, the Japan Society for the Promotion of Science, the European Molecular Biology Organization, the Juvenile Diabetes Research Foundation, the Strategic Young Researcher Overseas Visits Program for Accelerating Brain Circulation, the Broad Medical Foundation and the National Institutes of Health (grants AI095623 and DK35108).